Periapical pathology

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PRESENTED BY Dr EKTA GARG MDS 1 st YEAR DEPARTMENT OF CONSERVATIVE DENTISTRY & ENDODONTICS

Transcript of Periapical pathology

PRESENTED BY Dr EKTA GARG

MDS 1st YEARDEPARTMENT OF CONSERVATIVE DENTISTRY &

ENDODONTICS

Consists of cementum, pdl and alveolar process.

CEMENTUM

Mineralized, avascular connective tissue covering the roots of the teeth.

Consists of 3 different types-• Acellular afibrillar cementum• Acellular extrinsic fiber

cementum• Cellular intrinsic fiber

cementum

Cemental matrix consists of growth factors such as IGF-1, FGFs, EGF, BMPs, TGF-β and PDGF.

These factors r shown 2 b associated with cementoblast proliferation, migration, and differentiation during cementum wound healing.

PERIODONTAL LIGAMENT

Soft, specialized connective tissue that connects the cementum to the alveolar bone.

Contains heterogenous cell populations and extracellular matrix(ECM)

Cells include- osteoblasts, osteoclasts, fibroblasts, epithelial cell rests of malassez, macrophages, cementoblasts, & undifferentiated mesenchymal cells (stem cells)

ECM consists of collagen fibers, fibronectin, elastin, other non-collagenous proteins, & proteoglycans.

ALVEOLAR PROCESS

Forms the bony troughs containing the roots of the teeth.

Divided into-• Alveolar bone proper : lines the alveolus or the bony sockets

that house the roots of the teeth.• Supporting Alveolar bone : Cancellous(spongy) bone adjacent to

the alveolar bone proper covered by 2 outer tables of compact bone.

As a consequence of pathologic changes in the dental pulp, the root canal system can harbor numerous irritants. Egress of these irritants from infected root canals into the periradicular tissues can initiate formation and perpetuation of PERIRADICULAR LESIONS.

Depending on the nature and quantity of these irritants, as well as the duration of exposure of the periradicular tissues, a variety of tissue changes can occur.

When the irritants are transient in nature, the inflammatory process is short-lived and self-limiting.

However, with an excessive amount of irritants or persistent exposure, the nonspecific and specific immunologic reactions can cause destruction of periradicular tissues.

Radiographically, these lesions appear as radiolucent areas around the portal(s) of exit of the main canal or lateral and/or accessory canals.

Histologically, depending on their stage of development, the lesions contain numerous inflammatory cells such as polymorphonuclear neutrophil leukocytes (PMNs), macrophages, lymphocytes, plasma cells, mast cells, basophils, and eosinophils.

The interaction between the irritants and the host defensive mechanisms results in release of numerous mediators that curtail progression of infection and development of severe local infection (osteomyelitis) and systemic complication such as septicemia.

IRRITANTS

Can b divided into-• The LIVING irritants which include microorganisms and viruses.• The NON-LIVING irritants which include mechanical, thermal &

chemical irritants.

Mild to moderate injuries of short duration cause REVERSIBLE tissue damage and recovery of these tissues.

Persistent and/or severe injuries usually cause IRREVERSIBLE changes in the pulp and development of periradicular lesions.

Microbial Irritants

Includes-bacteria, bacterial toxins, bacterial fragments, and viruses

These irritants egress apically from the root canal system into the periradicular tissues and initiate inflammation and tissue alterations.

A number of studies have shown that pulpal and/or periradicular pathosis do not develop without the presence of bacterial contamination.

In addition to bacterial irritation, the periradicular tissues can be mechanically irritated and inflamed.

Physical irritation of periradicular tissues can also occur during root canal therapy if the canals are instrumented or filled beyond their anatomic boundaries.

Periradicular tissues can be irritated by impact trauma, hyperocclusion, endodontic procedures and accidents, pulp extirpation, overinstrumentation, root perforation, and overextension of filling materials.

The reaction of the periradicular tissues to noxious products of tissue necrosis, bacterial products, and antigenic agents from the root canal has been described by FISH.

Four well-defined zones of reaction found were-

• Zone of infection

• Zone of contamination

• Zone of irritation

• Zone of stimulation

CHIEF COMPLAINT: Pain on biting, pain wid swelling, pus discharge etc.

DENTAL HISTORY : Recurring episodes of pain, swelling wid discharge, swelling which reduces on its own.

OBJECTIVE EXAMINATION

• Xtraoral xamination- general appearance, skin tone, facial asymmetry, swelling, extraoral sinus, sinus tract, tender or enlarged cervical lymph nodes.

• Intraoral xamination- examination of soft tissues nd teeth to look 4 discolouration, abrasion, caries, restoration etc.

CLINICAL PERIAPICAL TESTS

1. PERCUSSION- indicates inflammation of the peridontium.

2. PALPATION- determines how far the inflammatory process has extended periapically.

3. PULP VITALITY-• Thermal tests- includes heat and cold testing• Anesthetic testing• Test Cavity• Electrical pulp testing

4. PERIODONTAL XAMINATION-• Probing- determines the level of connective tissue attachment.

• Mobility- determines the status of pdl.

5. RADIOGRAPHIC XAMINATION-• Loss of lamina dura apically• Radiolucency at apex regardless of cone angle nd usually resembles

a hanging drop.• Cause of pulp necrosis is usually evident.

WHO classification of periradicular tissues

CODE NUMBER CATEGORY

K04.4 Acute apical periodontitisK04.5 Chronic apical periodontitis

(apical granuloma)K04.6 Periapical abscess with sinus

(dentoalveolar abscess withsinus, periodontal abscess

of pulpal origin)K04.60 Periapical abscess with sinus

to maxillary antrumK04.61 Periapical abscess with sinus

to nasal cavity

CODE NUMBER CATEGORY

K04.62 Periapical abscess with sinus to oral cavity

Ko4.63 Periapical abscess with sinus to skin

Ko4.7 Periapical abscess with out sinus

Ko4.8 Radicular cyst(apical periodontalcyst, periapical cyst)

Ko4.80 Apical & Lateral cystKo4.81 Residual cystKo4.82 Inflammatory Paradental cyst

GROSSMAN’S CLASSIFICATION

Acute Periradicular disease(a) Acute alveolar abscess(b) Acute apical periodontitis(symptomatic periodontitis)

- Vital- Non Vital

(c) Acute exacerbation of chronic apical periodontitis(phoenix abscess)

Chronic periradicular diseases(a) Chronic apical periodontitis

- chronic alveolar abscess- cystic apical periodontitis

(b) Persistent apical periodontitis Condensing osteitis External root resorption Diseases of the periradicular tissues of non-endodontic origin

WEINE’S CLASSIFICATION

Painful pulpoperiapical pathosis(a) Incipient acute apical periodontitis(b) Advanced acute apical periodontitis

- Acute Periapical abscess- Phoenix abscess - Subacute Periapical abscess

Non painful Periapical pathosis (a) Condensing ostestis(b) Incipient chronic apical periodontitis(c) Advanced chronic apical periodontitis

- Periapical granuloma- Chronic Periapical abscess- Periapical cyst

INGLE’S CLASSIFICATION

Painful pulpoperiapical pathosis(a) Acute apical periodontitis(b) Advanced acute apical periodontitis

- Acute apical abscess - Phoenix abscess - Suppurative apical periodontitis

Non painful pulpoperiapical pathosis (a) Condensing ostetis(b) Chronic apical periodontitis

- Incipient- Advanced

(c) Chronic apical periodontitis- Periapical granuloma- Apical cyst- Suppurative apical periodontitis

Painful inflammation of the peridontium as a result of trauma, irritation, or infection through the root canal, regardless of whether the pulp is vital or nonvital.

Also referred to as symptomatic apical periodontitis.

Tooth is tender on percussion & pain can be severe making closure of the teeth difficult.

Etiology

IN VITAL TEETH-

Abnormal occlusal contacts

Recently inserted restoration extending beyond the occlusal plane

Wedging of a foreign object between the teeth such as a toothpick or food

Traumatic blow to the teeth

IN NONVITAL TEETH-

a) Sequelae of pulpal diseases, i.e., the diffusion of bacteria & noxious products from an inflamed or necrotic pulp.

b) Iatrogenic• Root canal instrumentation forcing bacteria or debris

inadvertently through the apical foramen• Forcing of irrigating irrigants or medicaments through the

apical foramen• Extension of obturating material through the apical foramen

to impinge on periapical tissue• Perforation of the root• Overinstrumentation during cleaning & shaping of root canals.

Signs & Symptoms

Tooth is tender on percussion & may b slightly sore

Dull, throbbing & constant pain

Tooth may feel extruded & patient would have pain on closure & mastication.

Negative or delayed vitality test

Radiographically, widening of the pdl space or a small area of rarefaction if a pulpless tooth is involved & may show normal periradicular structures if a vital pulp is present in the tooth.

HISTOPATHOLOGY

Inflammatory rxn in pdl

Dilation of blood vessels

Initiation of inflammatory response due to presence of polymorphonuclear leukocytes & round cells

Accumulation of serous exudate

Distension of Pdl & extrusion of tooth, slight tenderness

If continuous irritation occurs, loss of alveolar bone

Periodontitis caused due to trauma.

Widening of pdl space caused due to abnormal occlusal contacts

Widening caused due to orthodontic treatment

Periodontitis caused dueto carious xposure

TREATMENT

Determining the cause & relieving the symptoms.

Adjustment of high points (in hyperocclusion cases).

Removal of irritatants (in case of nonvital infected pulp)

When the acute phase has subsided, the tooth is treated by conservative means.

OUTCOME OF SYMPTOMATIC APICAL PERIODONTITIS

Spontaneous healing

Acute alveolar abscess

“Point” and open to the exterior (fistulation and sinus tract formation)

Lesion becomes asymptomatic and enters chronic phase.

An acute alveolar abscess is a localized collection of pus in the alveolar bone at the root apex of a tooth following death of pulp with extension of infection through apical foramen into periradicular tissue.

ETIOLOGY

• Trauma

• Chemical & mechanical irritation

• Bacterial invasion of dead pulp tissue.

CLINICAL FEATURES

Tenderness of the tooth relieved by continued slight pressure on the extruded tooth.

Severe, throbbing pain, with swelling of the overlying soft tissue.

No reaction to cold, heat or EPT.

As infection progresses, swelling becomes more pronounced & extends beyond the original site & tooth becomes more painful, elongated & mobile.

In case of max ant, swelling may extend to 1 or both the eyelids & in case of mand ant, swelling may involove the lower lip & chin.

In case of max post, cheek may swell 2 an immense size, distorting the facial structures & in case of mand post, swelling may xtend 2 ear or round the border of the jaw into the submaxillary region.

SYSTEMIC REACTIONS include-• Pt may appear pale, irritable & weakened due to pain & loss of

sleep.• Mild cases- slight rise in temp (99-100˚C)• Severe cases- temp above normal (102-103˚C)• Fever often preceded or accompanies by chills.• Intestinal stasis, manifesting orally by a coated tongue & foul

breath.• Headache & malaise

TREATMENT

Immediate treatment includes establishing drainage & controlling the systemic reaction.

LA is ineffective when injected into acutely inflamed tissue.

Conduction anesthesia may b administered to reduce the pain.

Hot saline rinses should b prescribed to assist drainage.

If the swelling is extensive, soft nd fluctuant, an incision through the soft tissue to the bone may b necessary.

If it is hard, can b converted to soft, fluctuant state by rinsing with hot saline solution 3-5 min at a time repeated every hr.

Antibiotics & analgesics can b prescribed as needed.

Finally, tooth shud b disoccluded slightly if extruded 4m its socket.

An acute inflammatory reaction superimposed on an existing chronic lesion, such as cyst or granuloma.

Acute exacerbation of a chronic lesion.

ETIOLOGY

1.When state of equillibrium in granuloma /cyst is upset by:• Influx of bacteria/necrotic products of high virulence and

antigenicity• Lowering of host defenses

2. Mechanical irritation during RCT.

CLINICAL FEATURES

Clinically often indistinguishable from periapical abscess.

Initially, tooth may b tender on palpation.

As inflammation progresses, tooth gets elevated from the socket & becomes sensitive.

Mucosa over the radicular area may appear red & swollen & sensitive to palpation.

Most commonly associated with initiation of root canal therapy.

Do not respond to vitality testing.

Radiographically, well defined periradicular lesion may b present.

Histopathologically, shows areas of liquefaction necrosis with disintegrated polymorphonuclear leukocytes & cellular debris surrounded by macrophages, lymphocytes, plasma cells in periradicular tissues.

Shud b differentiated from acute alveolar abscess through pt’s history, symptoms & clinical tests results.

TREATMENT

Establishment of drainage

Once symptoms subside, complete root canal treatment.

Symptomless sequelae of acute apical periodontitis.

May develop and enlarge insidiously without any subjective signs or symptoms.

Necrotic pulp gradually releases noxious agents with low grade pathogenecity or in low concentration.

Develops after inadequate root canal treatment.

Synonyms- asymptomatic apical periodontitis, periapical granuloma.

ETIOLOGY

• Death of the pulp followed by mild irritation of periapical tissue that stimulates a productive cellular reaction.

• Some cases preceded by chronic alveolar abscess.

CLINICAL FEATURES

Asymptomatic, discovered on routine radiographic xamination.

No pain on percussion

Associated tooth has a necrotic pulp therefore shud not respond to the electrical or thermal stimuli.

HISTOLOGICAL CHARACTERIZATION

• Periradicular granuloma or cyst.

The only accurate way to distinguish these two entities is by histologic examination.

A growth of granulomatous tissue continuous with the periodontal ligament resulting from death of the pulp and the diffusion of bacteria and bacterial toxins from the root canal into the surrounding periradicular tissues through the apical and lateral foramina.

Histologically, the periradicular granuloma consists predominantly of granulation inflammatory tissue with many small capillaries, fibroblasts, numerous connective tissue fibers, inflammatory infiltrate, and usually a connective tissue capsule

Occasionally, needle-like spaces (the remnants of cholesterolcrystals), foam cells, and multinucleated foreign body giant cells are seen in these lesions.

ZONES OF WELL ESTABLISHED GRANULOMA

TREATMENT

Root canal treatment is recommended.

Removal of cause of inflammation is usually followed by resorption of Granulomatous tissue & repair with trabeculated bone.

Pathological cavity containing fluid, semi fluid or gaseous material not created by accumulation of pus, frequently but not always lined by epithelium(Kramer 1974).

Radicular cyst are generally considered to be a direct sequelae of chronic apical periodontitis.

Not every lesion develops into cyst.

According to the studies 6-55% lesions are cyst.

There are two distinct categories of radicular cyst:-• Periapical true cyst• Periapical pocket cyst

ETIOLOGY

Acc to NAIR, cyst develops from dormant epithelial cell rests that proliferate probably under the influence of inflammatory cytokines & growth factors released by various cells residing in the lesion.

When proliferation occurs within the body of the granuloma, it plugs the body of the apical foramen which limits the egress of the bacteria.

Sometimes, epithelial plugs protrude out of the apical foramen resulting in a pouch connected to the root & continuous with the root canal.

Hypothesis related wid this growth-

a. Nutritional Deficient Theory-

• Periradicular inflammatory changes cause the epithelium 2 proliferate.

• As the epithelium grows into a mass of cells, the center loses the source of nutrition from the peripheral tissues.

• This leads to necrosis in the center & a cavity is formed which is lined by stratified squamous epithelium.

b. Abscess Theory-

• An abscess cavity is formed within the connective tissue & is then surrounded with proliferating epithelial tissue, thereby producing a cyst.

PRIAPICAL POCKET CYST

Originally designated as bay cyst.

Cyst contains an epithelial lined cavity that is open towards the root canal of the affected tooth.

initiated by the accumulation of neutrophils around the apical foramen in response to the bacterial presence in the apical root canal.

This forms a microabscess, that gets enclosed by the proliferating epithelium, forming a collar with epithelial attchment on contacting the root tip.

PERIAPICAL TRUE CYST

Characterized by cavities that are completely enclosed in epithelial lining and are totally independent of the root canal of the affected tooth.

Clinical features

• No symptoms associated with development of a cyst except incidental to necrosis of the pulp.

• May become large enough, however, to become obvious as a swelling.

• Pressure of the cyst may b sufficient to cause movement of the teeth, owing to accumulation of cystic fluid.

• If left untreated, may continue to grow at the expense of the max or mand.

HISTOPATHOLOGY

• Cavity is lined by stratified squamous epithelium.

• Surrounded by connective tissue that is infiltrated by lymphocytes, plasma cells, and polymorphonuclear neutrophils.

• Contains debris and eosinophilic material.

• Cholestrol clefts, macrophages, & giant cells also present in CT.

RADIOLOGICAL FEATURES:

Classically presents as round / ovoid radiolucency with sclerotic borders and associated with pulpally affected tooth / teeth.

If infection supervenes, the margins become indistinct, making it impossible to distinguish it from a periapical granuloma.

TREATMENT

• The treatment of choice is root canal therapy, followed by periodic observation.

• Surgery required when lesion fails to resolve or symptoms develop.

• Extraction in case of severe bone loss.

Periapical cyst

Radiographically, shows a well-circumscribed radiolucent periapical lesion with a partial sclerotic border, measuring more than 1 cm in diameter.

Histologically, shows the presence of an epithelial lining with underlying dense fibrocellular connective tissue stroma

Granuloma

Radiographically, shows a well-circumscribed radiolucent periapical lesion without a sclerotic border, measuring less than 1 cm in size.

Histologically, shows fibrocellular connective tissue stroma consisting of chronic inflammatory cell infiltrate (mainly lymphocytes and plasma cells) and endothelium-lined blood capillaries with red blood cells, fibroblasts, and collagen fibers.

Long standing, low grade infection of the periradicular alveolar bone.

Characterized by presence of an abscess draining through a sinus tract.

Synonyms- chronic suppurative apical periodontitis, asyptomatic apical abscess.

ETIOLOGY

• Source of infection is in the root canal.

• It is a natural sequelae of death of the pulp with extension of the infective process periapically, or may result from a pre-existing acute abscess.

CLINICAL FEATURES

• Tooth is asymptomatic or mildly painful.

• Detected only during radiographic examination or because of the presence of a fistulous tract, which can b either intraoral or extraoral.

• Exudate can also drain through the gingival sulcus of the involved tooth mimicking a periodontal lesion with a pocket.

• Vitality test is negative.

RADIOGRAPHICAL EXAMINATION

A radiograph is taken after the insertion of GP cone into the sinus tract which often shows the involved tooth by tracing the sinus tract to its origin.

At times, the sinus tract is several teeth away from the cause.

Radiograph shows diffuse area of rarefaction which fade indistinctly into normal bone.

The pdl is thickened.

HISTOPATHOLOGY

Some of the periodontal fibers at the root apex are detached or lost followed by destruction of apical periodontal ligament.

lymphocytes & plasma cells are generally found toward the periphery of abscessed area, with variable numbers of polymorphonuclear leukocytes at the center.

Fibroblast may start to form a capsule at the periphery.

TREATMENT

Elimination of infection in root canal.

Once this is accomplished & root canal is filled, repair of the periradicular tissues generally take place.

In case of smaller area of rarefaction, treatment is similar to that of a tooth with a necrotic pulp.

It is a rapidly spreading inflammation of the soft tissues characterized by diffuse pus formation.

This happens if an abscess is not able to establish drainage through the skin surface or into oral cavity.

Cellulitis arising from dental infection and spreading through soft tissues of head and neck can take various forms.

Mostly, infection spreads through tissue spaces like canine space, infratemporal space, pharyngeal space, buccal space, submental and submandibular space etc.

Two dangerous forms of cellulitis are –- Ludwig’s angina- Cavernous sinus thrombosis

TREATMENT

• Removal of the necrotic pulp.

• Extraction of the infected tooth.

• Incision & drainage of the swelling.

• In severe cases hospitalization required.

• Antibiotics & analgesics

Post treatment apical periodontitis in an endodontically treated tooth.

ETIOLOGY

• Anatomical complexity• Apical biofilms• Cholestrol clefts• Foreign body reaction to

gp• Cellulose granuloma• Periapical scar tissue

BACTERIOLOGY

E. Faecalis is the most consistently reported organism that can survive prolonged starvation & can grow as a monoinfection in endodontically treated teeth.

Studies have shown presence of yeast & candida albicans.

Gram+ cocci, rods & filaments, & Propioniobacterium have also been implicated.

Apical scar is an area at the apex of a tooth that fails to fill in with osseous tissue after endodontic treatment.

CHARACTERISTIC FEATURES

Bone structures are recognized within the rarefaction.

The periphery of the rarefaction may be irregular and may be demarcated by a compact bone border.

The rarefaction is often located asymmetrically around the apex.

The connection of the rarefaction with the periodontal space may be angular.

A surgical defect is that portion of bone that fails to form osseous tissue.

It is frequently seen periapically after root resection in which the site is filled with dense fibrous (collagen) tissue instead of bone.

It is an asymptomatic persistent radiolucency.

An extraction site can also form a surgical defect.

Approximately 75% of all surgically treated periapical radiolucencies require 1 to 10 years or longer for complete resolution. In the remaining 25%, complete healing does not occur.

Condensing osteitis is a reaction of bone induced by inflammation.

It occurs mainly at the apex of a tooth from an infected pulp.

The infection from tooth caries reaches the pulp and progresses to the apical tissues to produce a small periapical radiolucency called RAREFYING OSTEITIS.

The small rarefying osteitis may be either a periapical granuloma, a radicular cyst or an abscess.

The bone surrounding this rarefying osteitis becomes dense in order to prevent further spread of the lesion. This dense radiopacity surrounding the rarefying osteitis is called CONDENSING OSTEITIS.

CLINICAL FEATURES

Usually Asymptomatic

Discovered during routine radiographic examination.

Pulp of the involved tooth is nonvital.

RADIOGRAPHIC EXAMINATION

• The tooth involved may exhibit a large carious lesion or a largerestoration close to the dental pulp.

• The lesion shows a diffuse radiopacity surrounding asmall central radiolucency at the apex (or apices) of a tooth.

• It is the area of dense bone with reduced trabecular pattern.

HISTOPATHOLOGY

Appears as an area of dense bone with reduced trabecular pattern lined with osteoblasts.

Chronic inflammatory cells, plasma cells, & lymphocytes are seen in the scant bone marrow.

TREATMENT

Treatment consists of removing the infection either through toothextraction or root canal therapy.

CLASSIFICATION

Types of tooth resorption includes-

• External

a. External surface resorption

b. External inflammatory root resorption

c. External replacement resorption or ankylosis

• Internal

ETIOLOGY

• Trauma• Excessive forces• Granuloma• Cyst• Central jaw tumors• Impaction of teeth• Bleaching• Systemic diseases• If no cause is evident, the disorder is called as idiopathic

resorption.

CLINICAL FEATURES

Asymptomatic

On complete resorption, tooth may become mobile.

If extends into the crown, gives appearance of “pink tooth” as seen in internal resorption.

In case of replacement resorption or ankylosis, root is gradually replaced by bone, renders the tooth immobile, in infraocclusion, & with a high mettalic percussion sound.

RADIOGRAPHICAL EXAMINATION

• Concave or ragged areas on the root surface or blunting of the apex.

• Inflammatory root resorption caused by the pressure of a growing granuloma, cyst or tumor adjacent 2 the area of radiolucency.

• Areas of ankylosis hav a resorbed root with no pdl space & with bone replacing the defects.

TREATMENT

• Varies with etiology

• If extended by pulpal disease, root canal therapy.

• If due to excessive orthodontic forces, treatment of choice would b reducing those forces.

• In case of cervical root resorption, surgical xposure of the defect & restoration with a suitable rest material.

Odontogenic or

Nonodontogenic

• Dentigerous cyst

• Lateral periodontal cyst

• Odontogenic keratocyst

• Residual cyst

Bone Pathologies: fibro-osseous lesions

Periradicular cemental dysplasia

Osteoblastoma

Cementoblastoma

Cementifying & ossifying fibroma

Odontogenic tumours- ameloblastoma

• Central giant cell granuloma

• Nasopalatine duct cyst

• Globulomaxillary cyst

• Simple bone cyst

• Enostosis

Establishment of proper diagnosis is of utmost importance to carry out the effective clinical procedure for the benefit of patient .

Review after the treatment is also to be given importance .

Researches done and ongoing research has thrown light on various aspects untangling the puzzle which persisted for long.

So this knowledge can be used in the practice to make endodontic treatment a success when the controversy is going on about to pull out or salvage the tooth with implant coming strongly on the field of dentistry.